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1                                              LAP blockade is a general property of melanin pigments,
2                                              LAP depends upon reactive oxygen species (ROS) generated
3                                              LAP functions to limit the immune response and is critic
4                                              LAP initiated 20 years ago, has been described for all h
5                                              LAP is not developing, has not been adopted for intermed
6                                              LAP is required for efficient degradation of the engulfe
7                                              LAP is triggered by engagement of the TIM4 receptor by e
8                                              LAP neutrophils also displayed slower kinetics ( approxi
9                                              LAP was required for TLR9 trafficking into a specialized
10                                              LAP+ and LAP- fractions were analyzed by immunofluoresce
11                                              LAPs have a role in insect defense and act as a regulato
12 and peripheral blood were collected from: 34 LAP, 10 healthy siblings, and nine healthy unrelated con
13                 Distant recurrence was 14.6% LAP and 16.7% OPEN.Disease-free survival was impacted by
14       Local and regional recurrence was 4.6% LAP and 4.5% OPEN.
15                      There were 7881 (17.8%) LAP and 36,359 (82.2%) OPEN performed in an average of 4
16                     Nasal anti-CD3 induced a LAP(+) regulatory T cell that secreted high levels of IL
17 ll plants, whereas the stress-induced acidic LAPs (LAP-A) are expressed only in a subset of the Solan
18 P levels are significantly reduced, allowing LAP-mediated activation of the late promoter.
19 entional methods for leucine aminopeptidase (LAP) and pyrrolidonyl arylamidase (PYR) testing can be c
20                      Leucine aminopeptidase (LAP) is an essential proteolytic enzyme and potential bi
21 s, and the reference leucine aminopeptidase (LAP).
22                   l-Leucine aminopeptidases (LAPs) are implicated in the progress of many pathologica
23                     Leucine aminopeptidases (LAPs) are present in animals, plants, and microbes.
24        Three distinct clusters emerged among LAP participants: a high responder group (high level of
25  OPEN (243), with 462 eligible for analysis (LAP = 240 and OPEN = 222).
26 mage, it was shown that the tomato LAP-A and LAP-N and the Arabidopsis thaliana LAP1 and LAP2 are mol
27 es, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE.
28 teria infection on host Hsp60 expression and LAP-mediated bacterial adhesion, invasion, and transepit
29 tration results in expansion of Foxp3(+) and LAP(+) regulatory T cells (Tregs), suggesting oral deliv
30 duced a significant increase in Foxp3(+) and LAP(+) T cells in in vitro cultures.
31 different promoter activities of the HAP and LAP varieties.
32 gulatory elements differ between the HAP and LAP varieties.
33 ool to dissect the functions of the LAP* and LAP isoforms.
34                                     LAP+ and LAP- fractions were analyzed by immunofluorescence and m
35            Discordances between NucAmino and LAP occurred in 512 (16.9%) of the 3,029 sequences conta
36 ulosis to evade killing by NADPH oxidase and LAP.
37 the active form of C/EBP-beta (also known as LAP), acting as a critical molecular unit that controls
38 AP), latent TGF-beta and/or active TGF-beta (LAP/TGF-beta) is localized on the cell surface of Foxp3(
39 d and activate the latent form of TGF-beta1 (LAP-TGF-beta1).
40 ungal particles that are normally cleared by LAP.
41 ignment that was preferable to that found by LAP in that it was more likely to codon align insertions
42 0001), only 15% of patients were operated by LAP and intermediate (or major) resections were performe
43    The proportion of resections performed by LAP was inversely related to annual caseload.
44                              Phagocytosis by LAP macrophages was reduced approximately 40% compared t
45 y WTR (aHR 1.9 [1.4-2.6]) and black women by LAP (aHR 2.2 [1.4-3.5]).
46  a transposable 13-amino acid peptide called LAP (LplA Acceptor Peptide).
47 sing CD4(+) regulatory T cells (CD4(+)CD25(-)LAP(+) cells with upregulated IL-10 and transforming gro
48                                        CD4(+)LAP(+) T cells are hypoproliferative compared with CD4(+
49                     In vitro generated CD4(+)LAP(+)Foxp3(-) T cells were suppressive in vitro, inhibi
50    Adoptive transfer of orally induced CD4(+)LAP(+) Tregs ameliorated metabolic and cytokine abnormal
51 -6 abrogated the in vitro induction of CD4(+)LAP(+) T cells by STAT3-dependent inhibition of Lrrc32 (
52             The in vitro activation of CD4(+)LAP(-) T cells results in the generation of LAP(+) Tregs
53                                  These CD4(+)LAP(+) T cells lack Foxp3 but express TGF-betaR type II
54 ls are hypoproliferative compared with CD4(+)LAP(-) T cells, secrete IL-8, IL-9, IL-10, IFN-gamma, an
55 lent reliability towards monitoring cellular LAP activity in HepG2 cells.
56 ed in real-time active profiling of cellular LAP activity in HepG2 cells and effect of LAP inhibitor.
57 sible for the abnormal neutrophil chemotaxis LAP.
58 ), performed between 2008 and 2013, compared LAP and OPEN resection of stage II/III rectal cancer, wi
59  specific derivatization of azide-conjugated LAP in cells.
60 re we describe the consequences of defective LAP in vivo.
61  with a reasonable selectivity versus dizinc LAP.
62 cell surface receptor for the latent domain (LAP) of the multifunctional cytokine TGF-beta.
63               Here we report that C/EBPbeta (LAP) DNA binding is inhibited by N-terminal sequences an
64 y of another isoform of C/EBPbeta, C/EBPbeta-LAP, and might control liver biology through the regulat
65 ntify all patients who underwent an elective LAP or OPEN between 2007 and 2012.
66 ls in Caco-2 cells and consequently enhanced LAP-mediated L. monocytogenes adhesion but not invasion
67                                   The entire LAP completes in less than 20 min while using only a ten
68 Three-year LRFS for R0 resection was 86% for LAP cancer and 84% for RRC (P = 0.817).
69 g required for autophagy, is dispensable for LAP induced by uptake of microbes or dead cells.
70 dditional surface localization mechanism for LAP/TGF-beta, which may play an important role in contro
71 APs as well as suggesting new mechanisms for LAP action in the defense of solanaceous plants against
72 PAMPs and melanin removal, are necessary for LAP activation and fungal killing.
73 why its inhibitory activity is selective for LAP*.
74 rochemical signal is distinctly specific for LAP and free of other electroactive biological interfere
75 in 10 min and that it is highly specific for LAP fusion proteins over all endogenous mammalian protei
76  Of 100 exenterative operations, 55 were for LAP cancer and 45 for RRC.
77 l and highly sensitive fluorescent assay for LAPs based on substituted aminopyridines as fluorescent
78 ith increase in the frequencies of Foxp3(+), LAP(+), and GARP(+) T cells.
79 was lower in activated peripheral blood from LAP patients, we investigated the Maresin 1 (MaR1) biosy
80          By 10 months, colonies derived from LAP+ cells increased so that up to 35% of the liver was
81                             Macrophages from LAP patients had a lower level of expression of 12-lipox
82 ed with long-acting cabotegravir (GSK1265744 LAP) pharmacokinetic variability, the current study was
83 oth IM and SC locations following GSK1265744 LAP administration.
84 understand the biodistribution of GSK1265744 LAP and its associated pharmacokinetics.
85 to a maximum volume at 2days post-GSK1265744 LAP administration, while the Vehicle depot did not sugg
86  employed to examine the temporal GSK1265744 LAP biodistribution in rat following either IM or SC adm
87 of macrophages trafficking to the GSK1265744 LAP and Vehicle depot sites.
88                               The GSK1265744 LAP depot volume increased rapidly by day 2 in the IM in
89 resent in the depot region of the GSK1265744 LAP injected gastrocnemius while the Vehicle injected ga
90 ated a population of gastrointestinal-homing LAP(+)Foxp3(-) Treg cells.
91   However, the molecular mechanism(s) of how LAP/TGF-beta is anchored on the cell membrane is unknown
92              However, it remains unclear how LAP shapes both the activation and outcome of the immune
93 trusion and goblet cell exocytosis; however, LAP-induced cell junction opening may be an alternative
94 ve characterized a novel population of human LAP(+) Tregs that is different from classic CD4(+)Foxp3(
95 are due to defective engulfment and impaired LAP-mediated clearance of apoptotic germ cells as miR-47
96  and Capnocytophaga sp were most abundant in LAP.
97 cis together indicates sites of future BL in LAP.
98 ynergistic interaction of this consortium in LAP causation is possible and is the subject of ongoing
99                        Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like
100 old-higher endotoxin levels were detected in LAP plasma compared with that from healthy participants
101               For R0 resections only, DFS in LAP cancer was 76% and 57% in RRC (P = 0.212).
102 from diseased (DD) and healthy sites (DH) in LAP and from healthy sites in HS and HC and analyzed by
103              Nine mediators were elevated in LAP diseased sites as compared with healthy sites (TNFal
104 r systemic levels of endotoxin were found in LAP, which correlates with an exacerbated local inflamma
105        R0 rates were significantly higher in LAP cancer than in RRC (91% vs 62%, P = 0.001).
106    Hepatocyte-specific expression of hLAL in LAP-Tg/KO triple mice reduced the liver size to the norm
107 ponents of the autophagy pathway involved in LAP.
108 Expression of C/EBPbeta could be mimicked in LAP/LAP* isoform knockin DCs, whereas the short isoform
109  which the LTBP-binding cysteine residues in LAP TGF-beta1 were mutated to serine precluding covalent
110 , LPS-induced hyper-inflammatory response in LAP can be partially modulated by periodontal therapy.
111  However, the clinical effect of this SNP in LAP is ethnicity dependent, destructive (increases LAP i
112 was strongly associated and site-specific in LAP.
113  ethnicity dependent, destructive (increases LAP incidence), and complex with mechanisms still to be
114 lomyelitis, diabetes, and lupus) by inducing LAP(+) regulatory T cells.
115       Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated
116           When dying cells are injected into LAP-deficient mice, they are engulfed but not efficientl
117         Of interest, both the large isoform (LAP-2) and the small isoform (LIP) of C/EBP-beta can exe
118 -hLAL transgene with lal(-/-) knockout (KO) (LAP-Tg/KO) triple mice.
119 anoic acid, and the most efficiently labeled LAP clones were isolated by fluorescence activated cell
120 nts, whereas the stress-induced acidic LAPs (LAP-A) are expressed only in a subset of the Solanaceae.
121                            The neutral LAPs (LAP-N and its orthologs) are constitutively expressed an
122 ween mean ADC value of 12 lymphadenopathies (LAP) associated with inflammatory breast diseases (granu
123 enase ( approximately 30%) and reduced MaR1 (LAP versus healthy controls [HC], 87.8 +/- 50 pg/10(6) c
124  was largely restored in macrophages missing LAP components (Nox2, Rubicon, Beclin, Atg5, Atg7, or At
125  this assay was a useful tool for monitoring LAP activities in extracts from cancer cell lines, as we
126                                  The neutral LAPs (LAP-N and its orthologs) are constitutively expres
127       Here, we report the discovery of a new LAP biosynthetic gene cluster in the genome of Rhizobium
128 nes required for canonical autophagy but not LAP do not display defective dying cell clearance, infla
129 n of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-
130                For both sexes, quartile 4 of LAP carried increased risks for tobacco-exposed persons
131                               The ability of LAP to attenuate autoimmunity likely occurs through the
132 f the engulfed corpse, and in the absence of LAP, engulfment of dead cells results in increased produ
133 hibits NADPH oxidase-dependent activation of LAP by excluding the p22phox subunit from the phagosome.
134 is capable of monitoring in-situ activity of LAP in live cells.
135                   LCMS proteomic analysis of LAP-TAP-purified proteins from HeLa cells containing a t
136 th subsequent metalloproteolytic cleavage of LAP represents a major mechanism of TGF-beta activation
137                              Consequences of LAP deficiency include a decreased capacity to clear dyi
138 ar LAP activity in HepG2 cells and effect of LAP inhibitor.
139          Here, we describe the engagement of LAP upon uptake of apoptotic, necrotic, and RIPK3-depend
140 , and recombinant IL-2 induced expression of LAP on naive CD4(+) T cells, independent of Foxp3 or exo
141 L-10 or TGF-beta prevented the generation of LAP(+) Tregs and Foxp3(+) Tregs in vivo, and the LAP(+)
142 )LAP(-) T cells results in the generation of LAP(+) Tregs, which is further amplified by IL-8.
143 g mechanisms predicting the heterogeneity of LAP activity, severity, and response to treatment.
144                                The impact of LAP to immune regulation is best characterized in profes
145 acterial titers), and restored impairment of LAP phagocytes.
146  of the OPEN, P<0.0001) and the incidence of LAP biopsies increased after 2009.
147  Th2 responses, resulted in the induction of LAP(+) regulatory T cells and suppression of ongoing art
148 s was associated with a lack of induction of LAP(+) regulatory T cells.
149 lerance, strongly decreased the induction of LAP(+) Tregs.
150             A approximately 10(7) library of LAP variants was displayed on the surface of yeast cells
151                    Although the mechanism of LAP-A action is unknown, it has been presumed that LAP p
152 ped an in vitro model to study modulation of LAP(+) on CD4(+) T cells.
153  monitor cisplatin induced overexpression of LAP activity in HepG2 cells in presence and absence of b
154                            Overexpression of LAP is directly linked with some fatal physiological and
155 nerates a newly differentiated population of LAP(high)CD103(high) CD8(TGF-beta) Treg cells, which rep
156 arbamate (Leu-FC) for selective profiling of LAP activity in live cells.
157      Herein, we provide a detailed review of LAP and its known roles in the immune response and provi
158  These data provide insight into the role of LAP as a virulence factor during intestinal epithelial i
159                         More than a third of LAP+ fetal hepatocytes expressed ductal markers.
160 RNA against ANLN increased survival times of LAP-MYC mice, compared to mice given a control siRNA.
161 cheme was used to tag and image a variety of LAP fusion proteins in multiple mammalian cell lines wit
162          In plants, there are two classes of LAPs.
163           PHZ expands the known diversity of LAPs and may be used in the future as biocontrol agent f
164 ue to the compensatory function of two other LAP proteins, Erbin and Lano.
165                                       In our LAP participants, distinct patterns of LPS response were
166 s an exoprotease, leucine aminopeptidase (PA-LAP), which is coexpressed with several known virulence
167  by expressing the full-length proform of PA-LAP recombinantly in Escherichia coli (here termed, rLAP
168 read-out of a 5-parameter liver assay panel (LAP) on a portable, easy-to-use, fast and cost-efficient
169                     Long-Acting Parenterals (LAPs) have been used in the clinic to provide sustained
170 ow (enriched with light absorbing particles, LAPs) facilitate the study of particle loads on the fate
171 ic surface protein, leucine amino peptidase (LAP).
172 pressed both the latency-associated peptide (LAP) and the PD-1 receptor, two markers of functional Tr
173 des that express latency-associated peptide (LAP) on their cell surface but do not express Foxp3.
174 that express the latency-associated peptide (LAP), a membrane-bound TGF-beta1.
175 of TGF-beta, the latency-associated peptide (LAP), and having regulatory properties in human peripher
176 ession levels of latency-associated peptide (LAP), CD103, PD-1, PD-L1, and CTLA-4, as compared with p
177 at pro-TGF-beta, latency-associated peptide (LAP), latent TGF-beta and/or active TGF-beta (LAP/TGF-be
178 dependent CD4(+) latency-associated peptide (LAP)-positive Tregs by oral administration of anti-CD3 a
179  associated with latency-associated peptide (LAP).
180 -bound TGF-beta (latency-associated peptide [LAP]) and have been shown to play an important role in t
181 e substrate, called "LplA Acceptor Peptide" (LAP).
182        Linear azol(in)e-containing peptides (LAPs) comprise a subclass of RiPPs that display outstand
183 -induced localized aggressive periodontitis (LAP) in African-American adolescents has been documented
184          Localized aggressive periodontitis (LAP) is a distinct form of early-onset periodontitis lin
185 sed with localized aggressive periodontitis (LAP) present an in vivo phenotype with depressed chemota
186 cts with localized aggressive periodontitis (LAP) who had proximal bone loss but minimal proximal car
187 gent for localized aggressive periodontitis (LAP), an aggressive form of periodontal disease that occ
188 ren with localized aggressive periodontitis (LAP).
189 ponse in localized aggressive periodontitis (LAP).
190 ren with Localized Aggressive Periodontitis (LAP).
191 toxin in localized aggressive periodontitis (LAP).
192 etallo-aminopeptidases (MAPs), PfA-M1 and Pf-LAP.
193                In contrast, inhibition of Pf-LAP was lethal to parasites early in the life cycle, pri
194 e onset of Hb degradation suggesting that Pf-LAP has an essential role outside of Hb digestion.
195 li cells employ LC3-associated phagocytosis (LAP) by recruiting autophagy member proteins to clear ap
196                 LC3-associated phagocytosis (LAP) is a novel form of non-canonical autophagy where LC
197 monstrated that LC3-associated phagocytosis (LAP), a noncanonical autophagic process dependent on Rub
198 ophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles,
199  pathway termed LC3-associated phagocytosis (LAP), which promotes fungal killing.
200 ermed MAPLC3A (LC3)-associated phagocytosis (LAP), which results in optimal degradation of the phagoc
201 light chain 3 (LC3)-associated phagocytosis (LAP).
202  germ cells via LC3-associated phagocytosis (LAP).
203 ight-chain 3 (LC3)-associated phagocytosis" (LAP), lacked such defects.
204 athway called "LC3-associated phagocytosis" (LAP).
205                      Here we show that plant LAPs are bifunctional.
206  chaperones and a new function for the plant LAPs as well as suggesting new mechanisms for LAP action
207 xpression of latency-associated polypeptide (LAP)/TGF-beta and after adoptive transfer also their pro
208                                 In practice, LAP instantaneously hydrolyze the Leu residue of the sub
209 cludes Lm by occupying the surface presented LAP receptor, heat shock protein 60 and ameliorates the
210 d in patients with locally advanced primary (LAP) cancer and recurrent rectal cancer (RRC).
211 arteannuin B; the low artemisinin producers (LAPs), which include the 'Meise', 'Iran#8', 'Iran#14', '
212 ity index (VAI), lipid accumulation product (LAP), body adiposity index (BAI) and the waist-to-height
213 e considered the lipid accumulation product (LAP; [WC enlargement*triglycerides]).
214 d alignment program Local Alignment Program (LAP) using 115,118 human immunodeficiency virus type 1 (
215  cross-breeding of liver-activated promoter (LAP)-driven tTA transgene and (tetO)7-CMV-hLAL transgene
216 arboring deletions of the core LAT promoter (LAP) region.
217 teractors includes lamina-associated protein LAP-1, myocyte nuclear envelope protein Syne1, BetaM its
218 t not the liver-enriched activating protein (LAP) version, represses ATF4 transcription.
219 -enriched transcriptional activator protein (LAP) isoform of CCAAT/enhancer binding protein beta (C/E
220 rly, CEBPB-liver-enriched activator protein (LAP) isoform overexpression suppresses MYO18B transcript
221 is a receptor for Listeria adhesion protein (LAP) during Listeria monocytogenes infection.
222 P) to express the Listeria adhesion protein (LAP) from a non-pathogenic Listeria (L. innocua) and a p
223 demonstrated that Listeria adhesion protein (LAP) promotes adhesion to intestinal epithelial cells an
224 he interaction of Listeria adhesion protein (LAP) with the host cell receptor (heat shock protein 60)
225 beta propeptide [latency associated protein (LAP)], and a latent TGF-beta binding protein (LTBP).
226 -length (liver-enriched activating protein* (LAP*)) isoform but not the slightly shorter (LAP) isofor
227 sing localization and affinity purification (LAP)-tagged dynein/dynactin subunits from bacterial arti
228            The AAPC of the incidence of real LAP increased more than that of real OPEN (7.0% vs 1.3%)
229                                       REDUCE LAP-HF I (Reduce Elevated Left Atrial Pressure in Patien
230                                      (REDUCE LAP-HF Trial [REDUCE LAP-HF]; NCT01913613; and REDUCE LA
231 ial [REDUCE LAP-HF]; NCT01913613; and REDUCE LAP-HF Randomized Trial I [REDUCE LAP-HF I]; NCT02600234
232 eft Atrial Pressure in Heart Failure (REDUCE LAP-HF I), the first randomized controlled trial of a de
233 ssure in Patients with Heart Failure (REDUCE LAP-HF) study was an open-label, single-arm, phase 1 stu
234 and REDUCE LAP-HF Randomized Trial I [REDUCE LAP-HF I]; NCT02600234).
235                 (REDUCE LAP-HF Trial [REDUCE LAP-HF]; NCT01913613; and REDUCE LAP-HF Randomized Trial
236 d practice of laparoscopic liver resections (LAP), compared to open resections (OPEN).
237 sed to a 13-amino acid recognition sequence (LAP), catalyzed by a mutant of the Escherichia coli enzy
238 LAP*)) isoform but not the slightly shorter (LAP) isoform.
239 her, we concluded that inducible Ag-specific LAP(+) Tregs can suppress asthmatic lung inflammation an
240 eration, and transfer of sorted OVA-specific LAP(+) Tregs in vivo inhibited allergic eosinophilia and
241  Caco-2 cells more susceptible to subsequent LAP-mediated adhesion and translocation.
242 +)CD25(-) T cells, makes these cells surface LAP/TGF-beta-positive.
243                         Furthermore, surface LAP/TGF-beta forms a complex with the molecular chaperon
244 er, is not involved in GARP-mediated surface LAP/TGF-beta.
245 P78 reduced the expression levels of surface LAP/TGF-beta.
246                                  The surface LAP/TGF-beta contains high-glycosylated, furin-processed
247                 The optimal catalyst system (LAP 8-5-47) provided alpha-amino amides from an aldehyde
248                                TCRgammadelta+LAP+ cells express antigen presentation molecules and fu
249 + regulatory T cells, although TCRgammadelta+LAP+ cells do not themselves express Foxp3.
250              Identification of TCRgammadelta+LAP+ regulatory cells provides an avenue for understandi
251                    Here, we demonstrate that LAP is required for UV-induced immunosuppression and tha
252 P-A catalytic site mutants demonstrated that LAP-A chaperone activity was independent of its peptidas
253                                We found that LAP activation also requires the genetic, biochemical or
254 alizing Abs against cytokines, we found that LAP induction was decreased in the presence of IL-6 and
255 action is unknown, it has been presumed that LAP peptidase activity is essential for regulating wound
256      Collectively, these data suggested that LAP-A has a role in modulating essential defenses agains
257 onolayers than a lap mutant, suggesting that LAP is involved in transepithelial translocation, potent
258                                          The LAP receptor is a stress response protein, Hsp60, but th
259                                          The LAP(+) Tregs strongly suppressed naive CD4(+) T cell pro
260 me rural adults of Xinjiang was high and the LAP was an effective indicator for the screening of MetS
261  and WHtR were all greater than 0.7, and the LAP was the index that most accurately identified MetS s
262 +) Tregs and Foxp3(+) Tregs in vivo, and the LAP(+) Tregs could also be generated concomitantly with
263  of the DBR2 gene from varieties of both the LAP and the HAP groups.
264                      Its selectivity for the LAP* isoform also makes helenalin acetate an interesting
265 protein, Hsp60, but the precise role for the LAP-Hsp60 interaction during Listeria infection is unkno
266 he protein Scribble and its relatives in the LAP protein family provide a paradigm for this.
267  just upstream of the ATG start codon in the LAP varities, which might be the reason for the differen
268 f these, biopsies accounted for 29.9% of the LAP (7.3% of the OPEN, P<0.0001) and the incidence of LA
269 d Rubcn(-/-) mice to examine the role of the LAP pathway in mediating the UV-induced immunotolerant p
270 ice lacking any of several components of the LAP pathway show increased serum levels of inflammatory
271 al protein Scribble (Scrib), a member of the LAP protein family, is essential for epithelial apicobas
272 resting tool to dissect the functions of the LAP* and LAP isoforms.
273               Furthermore, disruption of the LAP-A hexameric structure increased chaperone activity.
274 lin acetate binds to the LAP* but not to the LAP isoform, explaining why its inhibitory activity is s
275 nt with this, helenalin acetate binds to the LAP* but not to the LAP isoform, explaining why its inhi
276 rthermore, inhibition of TSP1 binding to the LAP/TGF-beta complex decreased fibrosis in engineered ex
277 he clinical response to treatment within the LAP cohort.
278 ls of this response were observed within the LAP group.
279 escued by the conserved "LU" region of these LAP proteins.
280 pecific ligation of 10-azidodecanoic acid to LAP in cells, in nearly quantitative yield after 30 min.
281                     siRNAs were delivered to LAP-MYC mice, which develop hepatoblastoma, using lipid
282      In all, 486 patients were randomized to LAP (243) or OPEN (243), with 462 eligible for analysis
283 induced damage, it was shown that the tomato LAP-A and LAP-N and the Arabidopsis thaliana LAP1 and LA
284                        Upon transplantation, LAP+ late gestation fetal hepatocytes formed hepatic, en
285 in pathway have clinical utility in treating LAP and other oral diseases associated with infection, i
286 nds TSP1, which could potentially limit TSP1-LAP association and subsequent TGF-beta activation.
287 PRRs, for reasons that are poorly understood LAP does not substantially contribute to Mtuberculosis c
288 estine lamina propria, where they upregulate LAP, downregulate IFN-gamma via ATF-3 expression and acq
289                                 Assays using LAP-A catalytic site mutants demonstrated that LAP-A cha
290  apoptotic germ cells by Sertoli cells using LAP.Although phagocytic clearance of apoptotic germ cell
291                              The AUC of VAI, LAP and WHtR were all greater than 0.7, and the LAP was
292                           The 2-year DFS was LAP 79.5% (95% confidence interval [CI] 74.4-84.9) and O
293 phagocytes, in particular macrophages, where LAP has instrumental roles in the clearance of extracell
294 culation on the putative mechanisms by which LAP may regulate immune function, perhaps through the me
295 systemic levels of endotoxin associated with LAP.
296                 Through its association with LAP, TGF-beta is maintained in a latent form that must b
297 ree of systemic diseases, and diagnosed with LAP.
298                  Fifty-nine individuals with LAP were treated by mechanical debridement and systemic
299     In primary neutrophils from persons with LAP, PDK1 expression and activation levels were signific
300 ) loads are lower in snowpacks enriched with LAPs and are attributed to reductions in snowpack albedo

 
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